There are a number of hearing disorders which cause a great deal of suffering to mankind and various attempts have been made to relieve them.
Tinnitus
Tinnitus is the perception of sound in the human ear in the absence of corresponding external sound(s). Tinnitus can be perceived in one or both ears or in the head. It is usually described as a ringing noise, but in some patients it takes the form of a high pitched whining, buzzing, hissing, humming, or whistling sound, or as ticking, clicking, roaring, “crickets” or “tree frogs” or “locusts”, tunes, songs, or beeping. It has also been described as a “whooshing” sound, as of wind or waves. Tinnitus is not itself a disease but a symptom resulting from a range of underlying causes, including ear infections, foreign objects or wax in the ear, and injury from loud noises. Tinnitus is also a side-effect of some oral medications, such as aspirin, and may also result from an abnormally low level of serotonin activity.
The sound perceived may range from a quiet background noise to one that can be heard even over loud external sounds. The term “tinnitus” usually refers to more severe cases. Heller and Bergman (1953) conducted a study of 80 tinnitus-free university students placed in an anechoic chamber and found that 93% reported hearing a buzzing, pulsing or whistling sound. Cohort studies have demonstrated that damage to hearing from unnatural levels of noise exposure is very widespread in industrialized countries.
Because tinnitus is often defined as a subjective phenomenon, it is difficult to measure using objective tests, such as by comparison to noise of known frequency and intensity, as in an audiometric test. The condition is often rated clinically on a simple scale from “slight” to “catastrophic” according to the practical difficulties it imposes, such as interference with sleep, quiet activities, or normal daily activities. For research purposes, the more elaborate Tinnitus Handicap Inventory is often used. In a minority of cases, a clinician can perceive an actual sound (e.g., a bruit) emanating from the patient's ears. This is called objective tinnitus. Objective tinnitus can arise from muscle spasms that cause clicks or crackling around the middle ear. Some people experience a sound that beats in time with the pulse (i.e. pulsatile tinnitus). Pulsatile tinnitus is usually objective in nature, resulting from altered blood flow or increased blood turbulence near the ear (such as from atherosclerosis or venous hum, but it can also arise as a subjective phenomenon from an increased awareness of blood flow in the ear. Rarely, pulsatile tinnitus may be a symptom of potentially life-threatening conditions such as carotid artery aneurysm or carotid artery dissection. The basis of quantitative measurement of tinnitus relies on the brain's tendency to select out only the loudest sounds heard. Based on this tendency, the amplitude of a patient's tinnitus can be measured by playing sample sounds of known amplitude and asking the patient which he or she hears. The tinnitus will always be equal to or less than sample noises heard by the patient. This method works very well to gauge objective tinnitus (see above.) For example: if a patient has a pulsatile paraganglioma in his ear, he will not be able to hear the blood flow through the tumor when the sample noise is 5 decibels louder than the noise produced by the blood. As sound amplitude is gradually decreased, the tinnitus will become audible, and the level at which it does so provides an estimate of the amplitude of the objective tinnitus.
Objective tinnitus, however, is quite uncommon. Often patients with pulsatile tumors will report other coexistent sounds, distinct from the pulsatile noise, that will persist even after their tumor has been removed. This is generally subjective tinnitus, which, unlike the objective form, cannot be tested by comparative methods. If a subject is focused on a sample noise, they can often detect it to levels below 5 decibels, which would indicate that their tinnitus would be almost impossible to hear. Conversely, if the same test subject is told to focus only on their tinnitus, they will report hearing the sound even when test noises exceed 70 decibels, making the tinnitus louder than a ringing phone. This quantification method suggests that subjective tinnitus relates only to what the patient is attempting to hear. Patients actively complaining about tinnitus could thus be assumed to be people who have become obsessed with the noise. This is only partially true. The problem is involuntary; generally complaining patients simply cannot override or ignore their tinnitus. The noise is often present in both quiet and noisy environments, and can become quite intrusive to their daily lives. Subjective tinnitus may not always be correlated with ear malfunction or hearing loss. Even people with near-perfect hearing may still complain of it. Tinnitus may also have a connection to memory problems, anxiety, fatigue or a general state of poor health.
One of the possible mechanisms relies in the otoacoustic emissions. The inner ear contains thousands of minute hairs which vibrate in response to sound waves and cells which convert neural signals back into acoustical vibrations. The sensing cells are connected with the vibratory cells through a neural feedback loop, whose gain is regulated by the brain. This loop is normally adjusted just below onset of self-oscillation, which gains the ear spectacular sensitivity and selectivity. If something changes, it's easy for the delicate adjustment to cross the barrier of oscillation and tinnitus results. This can actually be measured by a very sensitive microphone outside the ear.
Other possible mechanisms of how things can change in the ear is damage to the receptor cells. Although receptor cells can be regenerated from the adjacent supporting Deiters cells after injury in birds, reptiles, and amphibians, in mammals it is believed that they can be produced only during embryogenesis. Although mammalian Deiters cells reproduce and position themselves appropriately for regeneration, they have not been observed to trans-differentiate into receptor cells except in tissue culture experiments. Therefore, if these hairs become damaged, through prolonged exposure to excessive decibel levels, for instance, then deafness to certain frequencies occurs. In tinnitus, they may falsely relay information at a certain frequency that an externally audible sound is present, when it is not.
The mechanisms of subjective tinnitus are often obscure. While it is not surprising that direct trauma to the inner ear can cause tinnitus, other apparent causes (e.g., temporomandibular joint disorder, (TMJ) and dental disorders) are difficult to explain. Recent research has proposed that there are two distinct categories of subjective tinnitus: otic tinnitus, caused by disorders of the inner ear or the acoustic nerve, and somatic tinnitus, caused by disorders outside the ear and nerve but still within the head or neck. It is further hypothesized that somatic tinnitus may be due to “central crosstalk” within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.
While most discussions of tinnitus tend to stress physical mechanisms, there is strong evidence that the level of an individual's awareness of their tinnitus can be stress-related, and so should be addressed by improving the state of the nervous system generally, using gradual, unobtrusive, long-term treatments.
While there are a few effective treatments for objective tinnitus, there is no methodoligical array of solutions for subjective tinnitus.
Tinnitus can have many different causes, but most commonly results from otologic disorders—the same conditions that cause hearing loss. The most common cause is noise-induced hearing loss, resulting from exposure to excessive or loud noises. Ototoxic drugs can cause tinnitus either secondary to hearing loss or without hearing loss, and may increase the damage done by exposure to loud noise, even at doses that are not in themselves ototoxic.
Howard, III, et al. in U.S. Pat, Nos. 6,456,886 and 5,697,975 describe a neural prosthetic device for reducing or eliminating the effects of tinnitus that includes a stimulation device and an electrode arranged in the primary auditory cortex. Mino in U.S. Pat. No. 5,788,656 describes an electronic stimulation system for treating tinnitus. It includes a probe that is placed at a site in proximity to the cochlea of the inner ear whereby the probe vibrations are transmitted to the cochlea. Wagner in U.S. Pat. No. 5,922,016 describes an apparatus for electric stimulation and diagnostics of auditory nerves of a human being that includes a stimulator detachably secured to a human being for sending a signal into a human ear, and an electrode placed within the human ear and electrically connected to the stimulator by an electric conductor for conducting the signals from the stimulator into the ear. A control unit is operatively connected to the stimulator for instructing the stimulator as to characteristics of the generated signals being transmitted to the ear. The electrodes that are placed within the auditory meatus are formed by a body of electrically conducting material such as e.g. graphite, metal or the like, and connected via an electric conductor to the stimulator, whereby the conductor is secured in place by an enveloping plastic body of elastically deformable material which bears upon the inside wall of the auditory meatus and which may also be used for sealing the auditory meatus. When being placed in the middle ear, preferably upon the promontory, Wagner describes the electrode in form of a body of electrically conducting material such as graphite, metal or the like, which is situated at the end of an insulated metal rod with electrical conduction. The metal rod is formed preferably in crank-like manner and is secured in place by an enveloping plastic body of elastically deformable material that bears upon the inner wall of the auditory meatus. Such a placement is claimed to be particularly effective to stimulate the auditory nerves.
Faltys et al. in U.S. Pat. No. 6,157,861 describe self-adjusting cochlear implant system and method which uses an implanted middle ear electrode to determine the middle ear reflex response. Rubinstein in U.S. Pat. No. 6,295,472 describes a method for generating pseudospontaneous activity in an auditory nerve and a system for treatment of tinnitus, comprising an adaptor that modifies a pseudospontaneous signal and an electrical contact adapted to be affixed nearby the cochlea.
Rubinstein et al. in U.S. Pat. No. 6,631,295 describe a method of diagnosing whether a human is a candidate for tinnitus reduction using a neural prosthetic. Di Mina et al. in U.S. Pat. No. 6,210,321 describe an electronic stimulation system for treating tinnitus. The system includes an electrodynamically-actuated diaphragm and probe assembly acting as an applicator to cause the probe to vibrate. The probe is placed at a site in proximity to the cochlea.
Zilberman et al. in U.S. Pat. App. No. 20010053872 describe a hearing aid comprised of conventional cochlear implant electronics implanted in the middle ear and coupled to an actuator configured to mechanically vibrate the middle ear ossicles. Stockert et al, in U.S. Pat. App. No. 20020019668 describe a hearing system for rehabilitation of a hearing disorder, comprising an output member for stimulating, via a passive coupling element, an ossicle of a middle ear.
Leysieffer et al. in U.S. Pat. App. No. 20020029070 describe an implantable system for rehabilitation of a hearing disorder with output-side electromechanical transducers for stimulation of the fluid-filled inner ear spaces. Leysieffer in U.S. Pat. App. No. 20020051550 describes hermetically sealed housing for an implantable medical device with separation wall which divides the housing to two chambers.
Goldsmith et al. in U.S. Pat. App. No. 20020099421 describe a transcanal, transtympanic cochlear implant system comprising a first component for removable positioning within the auditory canal, and a second component for implantation within the middle ear space, comprising an insulated receiver coil disposed between second and third bones, and a wire mesh electrode located within the receiving coil functioning as a ground electrode.
Based on the abovementioned prior art, it is evident that the middle ear has been previously conceived as a possible site for coupling mechanical vibrations to the (bony) conductive chain of the ear. This type of stimulation would probably be more suitable for hearing disorders that are classically categorized as conductive.
Meniere's Disease
Also called idiopathic endolymphatic hydrops, it is a disorder of the inner ear. Although the cause is unknown, it probably results from an abnormality in the fluids of the inner ear. Meniere's disease is one of the most common causes of dizziness originating in the inner ear. In most cases only one ear is involved, but both ears may be affected in about 15% of patients. Meniere's disease typically starts between the ages of 20 and 50 years. Men and women are affected in equal numbers. Usually, in case vertigo attacks are not controlled by conservative measures and are disabling, one of the following surgical procedures might be recommended:    a. The endolymphatic shunt or decompression procedure is an ear operation that is usually preserves hearing. Attacks of vertigo are controlled in one-half to two-thirds of cases, but control is not permanent in all cases. Recovery time after this procedure is short compared to the other procedures.    b. Selective vestibular neurectomy is a procedure in which the balance nerve is cut as it leaves the inner ear and goes to the brain. Vertigo attacks are permanently cured in a high percentage of cases, and hearing is preserved in most cases.    c. Labyrinthectomy and eighth nerve section are procedures in which the balance and hearing mechanism in the inner ear are destroyed on one side. This is considered when the patient with Meniere's disease has poor hearing in the affected ear. Labyrinthectomy and eighth nerve section result in the highest rates for control of vertigo attacks.Dizziness
A vague term describing various sensations, including a subjective feeling of uncertainty, postural instability, or motion in space. It also encompasses other sensations (e.g. light-headedness, wooziness, near fainting). The elderly often use the term even more broadly to include weakness, fatigue, and myriad other symptoms. Dizziness can be classified, somewhat arbitrarily, as acute (present for <1 month) or chronic (present for >1 month). Because the causes, diagnosis, and treatment of acute dizziness are similar for all adults, this chapter discusses only chronic dizziness and postural instability. The prevalence of chronic dizziness among the elderly ranges from 13 to 30%.
Dizziness is divided by history of sensation into five categories: (1) vertigo: a rotary motion, either of the patient with respect to the environment (subjective vertigo) or of the environment with respect to the patient (objective vertigo), the key element being the perception of motion; (2) disequilibrium (unsteadiness, imbalance, gait disturbance): a feeling (primarily involving the trunk and lower extremities rather than the head) that a fall is imminent; (3) presyncope (faintness, lightheadedness): a feeling that loss of consciousness is imminent; (4) mixed dizziness: a combination of two or more of the above types; and (5) nonspecific dizziness: a sensation of instability that does not fit readily into any of the previous categories.
Otosclerosis
As sound impinges upon the eardrum, it vibrates, causing the ossicles to move. The sound is then transmitted through to the inner ear. The chain of ossicles must be able to move freely for you to have normal hearing. The last bone in the chain is called the stapes. Otosclerosis causes new bone to grow over the stapes. This leads to a reduction in movement and eventually the bone becomes fixed. This reduces the transfer of sound to your inner ear and causes hearing loss. In the early stages of otosclerosis, or when the condition is mild, a patient might not need any treatment. However, sodium fluoride tablets have been shown to help prevent the progression of otosclerosis, but only if the condition has affected the inner ear.
Hearing aids can be very helpful and will typically be recommended before any surgical intervention is considered. However, otosclerosis typically continues to progress and hearing aids will not stop you developing profound deafness in the long term.
The common surgical treatment for otosclerosis is called stapedectomy. This operation aims to improve hearing by replacing the stapes—one of the ossicles—with a piston. The piston helps to restore the movement of the ossicles, so transmitting sound into the inner ear. Most of the stapes bone is removed, leaving just the portion called the footplate, which sits in contact with the oval window. The oval window is the link between the middle and inner ear. A small hole is then drilled in the footplate and the piston is inserted so that it sits in contact with the oval window. At its other end, the piston is attached to the incus, the middle of the three ossicles. However surgery may not relieve the tinnitus, and in case the inner ear is also affected, surgery may not improve the hearing either.
Hearing Loss
Hearing loss occurs when there is loss of sound sensitivity produced by an abnormality anywhere in the auditory system. A wide variety of conditions can cause hearing loss, including otosclerosis, cholesteatoma, and others. While physicians can sometimes identify the causes of hearing loss, in some cases the causes are unknown, or idiopathic.
Conductive Hearing Loss
Conductive hearing loss occurs when sound waves are prevented from passing from the air to the fluid-filled inner ear. This may be caused by a variety of problems including buildup of earwax (cerumen), infection, fluid in the middle ear, a punctured eardrum, or fixation of the ossicles, as in otosclerosis. Other causes include scarring, narrowing of the ear canal, tumors in the middle ear, and perforation of the tympanic membrane. Once the cause is found and removed or treated, hearing is usually restored.
Sensorineural Hearing Loss
Sensorineural hearing loss develops when the auditory nerve or hair cells in the inner ear are damaged. The source may be located in the inner ear, the nerve from the inner ear to the brain, or in the brain. Sensorineural hearing loss, commonly referred to as “nerve deafness,” frequently occurs as a result of the aging process in the form of presbycusis, which is a gradual loss occurring in both ears. Tumors such as acoustic neuromas can lead to sensorineural hearing losses, as can viral infections, Meniere's disease, meningitis, and cochlear otosclerosis. Sensorineural hearing loss can also be the result of repeated, continuous loud noise exposure, certain toxic medications, or an inherited condition. Generally, it is non-reversible. Scientists have, however, made great progress in uncovering the genes responsible for a number of forms of congenital hearing impairments/deafness, and this genetic researchmay in time lead to therapies for some congenital causes of hearing loss. Sensorineural hearing loss may be further differentiated as sensory or neural. Sensory hearing loss refers to loss caused by abnormalities in the cochlea, such as by damage from noise trauma, viral infection, drug toxicity, or Meniere's disease. Neural loss stems from problems in the auditory (eighth cranial) nerve, such as tumors or neurologic disorders. While tumors in this nerve may be life threatening, they are also often curable.
Mixed Hearing Loss
A combination of both conductive and sensorineural hearing loss. Hearing loss may be partial or total. It may develop gradually or suddenly. People with hearing loss may experience difficulties hearing conversations, especially if there is background noise. Hissing, roaring, or ringing in the ears (tinnitus) occurs in some conditions, as may dizziness or problems with balance (vertigo). On the other hand, there is also plentiful prior art that teaches embodiments of direct electrical stimulation of the cochlea. These applications usually aim to address hearing disorders of a more sensoryneural nature A main down side to direct electrical stimuli of the cochlea is the relatively high invasiveness of the implantation procedure and the acute and longer-term risks that are related to having gone through such a procedure and having such a device in place. The underlining concept of currently commercially available cochlear implants is based on an electrode array implanted along the curls of the cochlea and stimulating the different areas of the cochlea that span the desired frequency spectrum. Therefore, a non specific current being directed from the middle ear at the cochlea without discrimination of its different regions will not be effective in contemporary hearing aids that are based on separate stimulation per frequency bands.
Direct electrical stimuli of the cochlea could be considered as a method for relieving tinnitus. A main down side to direct electrical stimuli of the cochlea is the relatively high invasiveness of the implantation procedure and the acute and longer-term risks that are related to having gone through such a procedure and having such a device in place.
The Eustachian tube (or auditory tube) is a tube that links the pharynx to the middle ear. In adults the Eustachian tube is approximately 35 mm long. Some modern medical books call this the pharyngotympanic tube. The Eustachian tube extends from the anterior wall of the middle ear to the lateral wall of the nasopharynx, approximately at the level of the inferior nasal concha. A portion of the tube (˜⅓) proximal to the middle ear is made of bone; the rest is composed of cartilage and raises a tubal elevation, the torus tubarius, in the nasopharynx where it opens. The Eustachian tube evidently represents a much less invasive implantation route, compared to contemporary methods for placing cochlear electrodes directly in the middle ear—risking infection and possibly irreversibly damage to sensitive sensory and other neural structures.
It is a long felt and unmet need therefore to provide an auditory implant system for treating a hearing disorder which is minimally invasive. Furthermore, such an implant system which provides electrical signals to the cochlea and is implanted via the Eustachian tubes would answer an unmet and long felt need.